(The original, long version of the article is available by clicking here.)

What if you found out that plain old vitamin K1 was just as good, maybe even better than the expensive K2, but it happens to be the best-kept secret? Are you familiar with Dumas' Iron Mask story, in which one of two twin princes is hidden in an iron mask while the other reigns supreme? Well, the situation with vitamin K is not unlike that: K1's iron mask is that it only regulates blood clotting and is well hidden from view. When found, it is claimed to be the result of some ill-conceived study... K1 has produced the effects of K2 in both animal and human studies, and in comparisons, it has beaten K2 hands down, yet we never hear about it... Nor do we hear that the modern western diet is actually very rich in K2 due to the consumption of processed industrial meat products, while the diet of indigenous peoples and our ancestors was practically devoid of K2, but had up to 100 times as much K1... Western people's K1 consumption has been reduced to a fraction and K2 has increased steeply in comparison to indigenous peoples and our ancestors... 

Contrary to custom, I'll start my article with the summary and conclusion (practical recommendation), as I presume many people might not want to wade through the tedious details... Those who get curious about the details after the summary may continue reading under the summary table... 

Summary and practical recommendations: 

In principle, 500-1000 mcg of K1 of moderate to good absorption per day seems sufficient in the long run. For vegetable-derived K1, this means it should be eaten with sufficient fat and preferably heat-treated, while from supplements, an oil-soluble or emulsified form should be taken with meals so that absorption is around 80% and the half-life is rather long. 

Some medicines (statins, bisphosphonates, coumarin derivatives) inhibit the conversion of K1 and MK-7 to K2 MK-4, so it is advisable to take MK-4 as well, at least 1500 mcg per day (after consulting your doctor.) D3, zinc, and magnesium enhance the conversion of K1 to K2. Vitamin A (retinol) and vitamin B6 also assist the effect of K2. It is worth minding sufficient consumption of these. 

To preserve the natural MK4/K1 ratio in our tissues and thus enhance the effect of vitamins K and prevent counterproductivity, if you take K2 MK-7, you should also take at least 3x as much K1, while if you take MK-4 you should also take at least the same amount of K1 so that K2 vitamins do not cause any problems. 

K1 is safe on its own, and unless its conversion is blocked by these drugs, K1 is the most potent of the K vitamins. Ideally, I recommend taking at least 500mcg of vitamin K1 daily in oil-soluble or emulsified form, but preferably 1000mcg. In addition to this, I also recommend optionally taking 100-200mcg of K2 MK-7, but no more. It may even be worth taking over 1000mcg of vitamin K1. 5mg a day seems ideal as in one study this amount (taken for 2-4 years) reduced cancer risk by a quarter and fracture risk by half. 

 

An excellent illustration of the transformation of vitamin K in the body from the chapter on vitamin K in the Pharmacology of Natural Medicines, 5th edition 2020 of the Textbook of Natural Medicines: 

And a great chart showing the absorption of 900 mcg K1 + 900 mcg MK-4 + 1600 mcg MK-9 in a healthy person when consumed dissolved the butter of a breakfast toast: 

Forms of vitamin K and their occurrence in nutrition  

Vitamin K3 (menadione) - While it is not found in food, all vitamin K, whether K1 or K2, is partially or fully broken down in the body to K3, which is then converted to K2. It is therefore a transitional form not used in food products. Yet, as it is particularly effective in increasing the body's vitamin K2 levels and is inexpensive, it is used in megadoses in the diets of industrially reared animals, and in normal doses in other diets such as dog food. The vitamin K2 content of meat and liver can be high in meat products, particularly in processed meat products, because of the mega-dose of K3 in their diet. Extremely high doses of K3 worsen the antioxidant status and for this reason, it is not approved for use in supplements for humans, which is a pity because even small doses are very good at increasing the body's K2 levels. 

Vitamin K1 has one type which is phylloquinone, also known as phytomenadione.  

Only one form of Vitamin K2 is found naturally in animals and humans in significant amounts, menaquinone-4 (MK-4). Very small amounts of longer-chain menaquinones can also be found in our liver, which are formed by intestinal bacteria mainly from vitamin K1 and stored in the liver. One of these is menaquinone-7 (MK-7). Various bacteria also produce all lengths between MK-5 and MK-14, conceivably MK-1/2/3 and menaquinone above MK-14, too.

Vitamin K1 is abundantly found in plant foods, but also in animal foods, only to a lesser extent. K2 practically does not occur in food except for aged cheeses, fermented soy (natto), and foods made from animals fed with mega-doses of vitamin K3-enriched food, in everything else it is found only in trace amounts.

Approach to the various forms of Vitamin K based on the diet of our ancestors and the people from natural tribes

Vitamin K1 occurs abundantly in the diet of people from natural tribes (on average approx. 1000 mcg per day). In addition, during our decisive "aquatic ape" evolutionary phase that took place on the East African ocean coast, for millions of years we could also eat "sea vegetables" with an extremely high vitamin K1 content, from which we could obtain up to 1 million mcg/day of K1 (in addition, they also contain high amounts of DHA). Whether it happened or not, in today's modern diet, our intake of vitamin K1 has decreased by more than a tenth, compared to what is typical for natural people. On the other hand, our intake of vitamin K2 has increased by about 10-100 fold, because food sources of K2 have practically only existed for a few hundred years: by far the richest sources are cheeses, fermented soy, but especially modern processed and other meat products. K2 content above 10 mcg/100 g has not yet been measured in any part of free-range and wild animals, only 1-2 mcg/100 g is typical. High K2 content in animal food was measured only where, compared to the animal's natural diet, they received approx. 100x times the amount of vitamin K in their food (in this case, poor-quality food is enriched with synthetic Vitamin K3 in mega-doses, as this is a much cheaper solution than feeding them normally) and possibly, in addition, due to the poor housing, eating feces may also be common for these animals. (Feces have a very high K2 content if vitamin K intake is high and thus eating feces further increases the K2 level in meat and all tissues). According to a recent measurement, foods made from such industrially reared pigs contain 300-500 mcg of K2/100 g, while their fresh meat also contains up to 100 mcg of K2, mainly in the form of MK-8/9/10/11, which are dominant in the feces. The liver pâté made from goose liver stuffed with K3-enriched corn also contains nearly 400 mcg of K2, but in the form of MK-4 (a stuffed goose does not regurgitate its feces), while its leg meat also contains 30 mcg of MK-4 (60 mcg was also measured in chicken legs /100 g). The practice of mega-dosing K3 in the meat industry thus results in high K2 levels in modern industrially produced meat products. Presumably, if the domesticated animal does not re-eat another animal's or its own feces very often, high levels of K3 supplementation will result in high MK-4 content in the meat, while if the animal eats feces frequently, it will get so much MK-8-11 with a very long half-life, that they could surpass the level of MK-4 in the meat.

Anyway, it seems pretty clear that no food that existed thousands of years ago could really have had a K2 content above 10 mcg/100 g, unless we consumed feces (e.g. the Hadza tribe sometimes make a soup from animal feces boiled with starchy tubers and spices). Apart from fecal consumption, however, we only had access to K2 in the form of MK-4, and it is unlikely that we would have been able to approach a daily intake of 100 mcg K2, which counts as nothing because MK-4 has no effect in doses below 600 mcg and presumably it doesn't even reach our bloodstream in such low amounts. The Yupik Inuit, who eat very little plant food and live almost exclusively on animal food, have been found to be particularly deficient in vitamin K, often not even having enough vitamin K in their bodies for the proper functioning of their blood clotting factor

In summary, the consumption of Vitamin K1 by modern humans has decreased to a fraction of our evolutionary intake, while the consumption of K2 has increased many folds.

This may also be surprising because the body of humans and animals contain much more MK-4 than K1, and contains no other form of K2. It follows that a lot of K1 alone is enough to ensure the body's optimal K2 level. How could this be?

Regardless of what type of vitamin K we swallow, a significant part of it is already transformed into K3 in the intestinal cells during its absorption (even if we consumed MK-4, it is also transformed into K3 first in part or in whole). The K3 thus created from K1 and K2 reaches the tissues via the bloodstream, where an enzyme called UBIAD1 converts them into K2 MK-4 (the K3). The portion that is not transformed into K3, reaches the tissues in an unchanged form and is incorporated as such, and later converted by the tissue into K3 and only after into MK-4 according to its own needs, but this process happens much more slowly since the UBIAD1 enzyme can convert K1 into K3, but it excels in the K3->MK-4 conversion. In addition, the liver can also convert K1 into K2 MK-4 (this is enhanced by vitamin D3). Moreover, in the case of K1, K2 is also formed from the unabsorbed part! Intestinal bacteria convert nearly 100% of vitamin K1 into K2 (MK-8/9/10, etc.) measured in modern western people, although not much of it gets back into the bloodstream beyond the liver, but this is presumably partly due to its low concentration -> with a higher K1 intake, the concentration can be increased and thus more K2 can be returned.

The bottom line is that many known mechanisms ensure the Vitamin K1->K2 conversion in humans and animals. Quite a few studies have been carried out, from which the conclusion can be drawn that the K1->K3->MK-4 conversion is efficient in both humans and mice, as is the production of K1->K2 (MK-8,9, etc.) in the intestines. In a study done in healthy people, they tried to establish that approximately how much can be converted from a high dose of K1 taken orally to K3 and then to K2 within 24 hours after its absorption and they came to the conclusion that 8-30% of the dose taken, which if we use the absorbed dose it means an approximately 50% absorption rate, which does not take into account that it is also transformed later on in the tissues and by intestinal bacteria

Tissues have their own ideal vitamin K ratio (MK-4/K1). In them, Vitamin K1 can be transformed into K2 (MK-4), but there are tissues that do not transform all of it because they prefer K1. Since K2 cannot be converted back to K1, excessive doses of K2 can disrupt the ratio, while K1 cannot. K1 increases the K2 level in the tissues to the same extent as K2 MK-4 itself, while maintaining the ideal MK-4/K1 ratio characteristic of the specific tissues

 

Utilization

The utilization of K2 MK-7 is the best, as almost the entire dose is fully utilized, while a maximum of 80% of vitamin K1 is. In doses below 600 mcg, MK-4 is probably not useful at all, while when taken in a dose of 1000 mcg dissolved in butter, it is utilized by a third as much as K1 consumed in the same manner. MK-4 is cleared from the blood the fastest (its half-life is approximately 4 hours), while the half-life of K1 and K2 MK-7 and MK-9 dissolved in oil and taken with food is approximately 6-7 hours, however, in the case of MK-7 and MK-9, there is a secondary half-life, i.e. after its level drops to half or a quarter, it only halves every 2 days. All this means that the effect of 200 mcg MK-7 corresponds to approximately 600 mcg of K1 and 1800 mcg of K2 to MK-4 if we accept that both K1 and MK-7 are able to transform into MK-4 as needed (K1 does not need to be all transformed, since the tissues also need K1, not only MK-4, but it is important for MK-7 to transform fully and that is exactly why there can be a problem if we take too much K2 without adequate K1)

If all that I have written so far is true, then studies conducted with K1 should show a similar or better health improving and disease risk-reducing effect than those with K2, especially in studies directly comparing K1 with K2. As you will find out this is exactly the case! As they say, the proof of the pudding is in the eating, but before that let's take a closer look at what studies are used to show that K1 is not effective:

• In-vitro studies: There is no need to even comment on this since K1 can only turn into K2 in a living organism..
• Rotterdam study and others: These are epidemiological studies, i.e. they are only able to show correlation, not a cause and effect relationship. Some of these studies found that those with the highest consumption of gourmet cheese on a food questionnaire test (source K2) had lower rates of certain cardiovascular risks than those with the lowest consumption of cheese. The difference was 14mcg K2 in their diet (7mcg MK-9 + 7mcg MK-4). The group consuming the least K1 consumed about 150 mcg of K1, while those consuming the most consumed about 300 mcg. More K1 only reduced the risk less than K2, which is why these studies are often referred to, however, from 300 mcg of K1, which is not taken as an oil-based supplement, but for example, as vegetables, only a little more is absorbed than what the liver needs, so it is not surprising that they did not find a big difference in the effect of very low and extremely low vitamin K1 consumption. What is more surprising is what is in these gourmet cheeses, or is it just that gourmets eat far less junk food? Since 2016, however, we have known that the consumption of processed meat products is associated with up to 10-20x as much K2 intake as the high consumption of cheese, but until now it was considered close to zero. For this reason, all similar K2 studies, where the K2 content of the industrial meat products was considered to be close to  0, can either be thrown in the trash or recalculated afterward. And all studies are like that. Later, in a more precisely organized study in Greece, it was found that in the participants with a higher (average 600 mcg) K1 intake, more types of cardiovascular problems were halved than in the Rotterdam study, moreover, the risk of cancer and total mortality was also significantly reduced ... And here K2 was examined simultaneously with K1, not just separately. Higher K2 intake was not found to be effective, even though it was higher than in the Rotterdam study and there were bigger differences, although this does not mean anything, since the high K2 content of meat products was not taken into account in this study either, so the corresponding statement regarding K2 is also incorrect here, however, the one regarding K1 is correct, since the K1 intake was sufficiently high, from which enough reached the tissues beyond the activation of the blood coagulation factors.

The conversion of K1 to K2 is inhibited by certain medications such as statins and bisphosphonates. It is also possible to point out that certain trials were conducted while taking such drugs, and in these cases, the competitor's leg was broken before the competition: They also used to point to such a mouse test, where the researchers simply wanted to prove that K1 must be able to transform into K2 (MK-4) to exert its anti-vascular calcification effect. Here, such a conversion blocking drug (Warfarin) was administered throughout the study, while the mice were given K1 or K2 MK-4 for months. K2 (MK-4) prevented vascular calcification, while K1 did not. That is, if K1 is not allowed to transform into K2 MK-4, then it has no effect. (It was not tested, but I am sure that MK-7 would not have had an effect either, since it also has to be transformed into MK-4). Later, in another study, mice with severe aortic and coronary atherosclerosis were given high doses of K1 or K2 (MK-4) without the conversion-blocking drug (about 50 mg/day in human terms). Both reversed and approximately halved the calcified plaque deposits in 6 months time. K1 was significantly more effective than MK-4, which may be because as they have measured in the tissues of the animals, MK-4 administration upset the ideal MK4/K1 ratio, while K1 administration maintained it while increasing tissue MK-4 by the same amount, as MK-4 itself.

Human trials:

After we have cleared the contradictions, let's look at what's most important: are these effects confirmed by human interventional studies

Their osteocalcin and MGP activating effect: The effect on the heart/vascular system, calcification, teeth, and skin depends on how well a type of vitamin K is able to activate MGP, while the effect on the skeletal system and teeth depends on how well they activate osteocalcin. All of these were activated best by K1 in human clinical trials and at a dose of only 500-1000 mcg. Similar good results have not yet been achieved with any amount of K2, the closest was once with 45,000 mcg of K2 (MK-4)...

Epidemiological studies have already been mentioned in connection with the Rotterdam study, but they are not even worth mentioning, as they are completely irrelevant, because they were calculated using wrong data, as it turned out a few years ago...

In placebo-controlled studies looking at the effect on bones, doses of vitamin K1 between 500 mcg and 5 mg were similarly effective as 45 mg (=45 thousand mcg) doses of MK-4. MK-7 was effective at 100-180 mcg, although significantly less so than K1 or MK4. MK-7 was not, but both K1 and K2 were able to not only slow/stop, but also reverse osteoporosis. There are several studies on MK-4, but all of them were 45 mg doses, while the highest dose of K1 was 5 mg, which was studied at length on the bones. The fact that K1 is just as effective and sometimes more effective than K2 MK-4 even at such a lower dose can be explained not only by maintaining the correct tissue ratio but also by its better absorption

In examining the effects on the cardiovascular system, K1 turned out to be the most effective in doses between 0.5 and 5 mg, although MK-4 also had a positive effect in doses of 45 mg, but to a lesser extent. MK-7 has not been found in any studies to prevent or improve calcification or any other cardiovascular problem. In fact, in the most recent study, where the most accurate measurement method to date was used to determine calcification, they found that taking 360 mcg of K2 MK-7 increased calcification in blood vessels by 10% compared to placebo, instead of decreasing it. (In the case of MK-7, this is already an impractically high dose, because even people with the highest dietary MK-7 intake in the world consume less than 200 mcg per day on average, and knowing its slow half-life, such a dose accumulates when taken daily and can disrupt the tissue MK4/K1 ratio)

Head-to-head comparison

Of course, they can only be properly compared if they are examined head-to-head in the same study, in the same setting, and randomized between the same subjects. Fortunately, there are 2 such studies, after which they were never done again, as it is financially very painful for the manufacturers of Vitamin K2, that as it turned out the 100 times cheaper vitamin K1 is more effective than the expensive K2... In one of these studies, the effect of 45mg of K2 MK-4 per day was compared with 1mg of vitamin K1 per day. They performed equally well, and K1 even had a slight edge (both prevented BMD changes, but 1mg K1 activated osteocalcin a little more than 45mg K2

In another study, only 100 mcg of K1 or K2 MK-7 was added to a diet that already contained 100-150 mcg of K1. K1 significantly increased the bone density of the lower part of the spine (3x more) than K2, while their other effects were the same, for example, they both reduced soft tissue calcification.

Finally, it is also worth mentioning the studies done on cancer: Vitamin K3 has the strongest anti-tumor effect, which is converted from all types of vitamin K in a similar manner. For this reason, also K1 seems to be the most practical and indeed the best here, since it is the cheapest, has at least 3x better absorption than K2 MK-4, and although MK-7 is 3x better absorbed than K1, it is 100x more expensive, and its 360 ​​mcg dose can already be risky while mg doses would be needed in this case.

In one study, 440 post-menopausal women took 5 mg of K1 or placebo daily for 4 years. This reduced the incidence of cancer to only a quarter of that of the placebo group, while also halving the number of bone fractures! This is the only placebo-controlled study on the relationship between K1 and cancer. This is roughly the same as the effect that has been observed in several studies with doses of 45mg or higher of MK-4 per day

In addition, there is also 1 study of K1 and K2 MK-4, where their doses of 40-45mg or higher caused a reduction in tumor size or even complete remission. In one K1 study, with approximately 50 subjects stabilization of the condition was achieved in 75% of them, while tumor size reduction was achieved in 15%. These were end-stage, metastatic, inoperable cases of liver cancer, so this is a surprisingly good result.

[The cover image of the note shows natto. 100 grams contains 900 μg of vitamin K, which is 9 times the recommended daily intake value.]